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PubMed1981

Enhancement of mammary tumorigenesis by dietary selenium deficiency in rats with a high polyunsaturated fat intake.

The effect of selenium depletion on mammary tumorigenesis following dimethylbenz[a]anthracene administration was examined in female Sprague-Dawley rats that were fed different levels and types of fats. Four basal diets deficient in selenium were used: (a) 1% corn oil; (b) 5% corn oil; (c) 25% corn oil; and (d) a high saturated fat diet containing 1% corn oil and 24% hydrogenated coconut oil. The comparable selenium-adequate diets were obtained by adding 0.1 ppm of selenium to each of the basal diets. In animals that received an adequate supplement of selenium, an increase in fat intake was accompanied by an increased tumor incidence when corn oil was used in the diets. A high saturated fat ration, on the other hand, was much less effective in this respect. Only in those rats that were maintained on a high polyunsaturated fat diet (25% corn oil) did selenium depletion result in a further increase in tumor incidence and tumor yield. Such an augmentation was not observed in animals given either a 1 or a 5% corn oil ration or a diet rich in saturated fat. Regardless of selenium status, almost all of the tumors found were adenocarcinomas. An enhancement of tumorigenesis as a result of selenium deficiency in rats fed the 1% corn oil regimen was detected provided a high dose of dimethylbenz[a]anthracene was used, suggesting that alterations in dimethylbenz[a]anthracene metabolism might be involved under this condition. The antioxidant property of selenium is discussed as a possible mechanism by which selenium protects against tumorigenesis, especially in animals with a high polyunsaturated fat intake.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1981

Prophylaxis of mammary neoplasia by selenium supplementation in the initiation and promotion phases of chemical carcinogenesis.

The present study was designed to determine the chemopreventive effect of dietary selenium supplementation in the initiation or promotion phase of 7,12-dimethylbenz[a]anthracene-induced mammary carcinogenesis in rats fed a high-fat diet. Control animals received 0.1 ppm of selenium (as sodium selenite), while experimental groups were supplemented with 5 ppm of selenium for various periods of time: -2 to +24, -2 to +2, +2 to +24, +2 to +12, +12 to +24, and -2 to +12. The time of 7,12-dimethylbenz[a]anthracene administration (50 days of age) was taken as Time 0; minus and plus signs represent the time in weeks before and after 7,12-dimethylbenz[a]anthracene administration, respectively. The following conclusions were drawn from the results: (a) selenium can inhibit both the initiation and promotion phases of carcinogenesis; (b) a continuous intake of selenium is necessary to achieve maximal inhibition of tumorigenesis; (c) the inhibitory effect of selenium in the early promotion phase is probably reversible; and (d) the efficacy of selenium is attenuated when it is given long after carcinogenic injury. In addition, the present investigation also assessed the effectiveness of selenium in inhibiting the reappearance of mammary tumors that had regressed after ovariectomy. By supplementing tumor-bearing animals with 5 ppm of selenium in the diet immediately after endocrine ablation, it was found that tumors reappeared at a slower rate compared to the controls. The data suggested that selenium is not only effective in chemoprevention but can also be used as an adjuvant chemotherapeutic agent.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1983

Selenium concentration and glutathione peroxidase activity in normal and neoplastic development of the mouse mammary gland.

This study was divided into three experiments. (a) The levels of selenium and glutathione peroxidase (GSH-PX) activity were determined for various developmental states of the mammary gland: normal (virgin, pregnant, and lactating); preneoplastic hyperplastic outgrowth lines; and neoplastic mammary tissues. Tissues from the pregnant and lactating mice had higher selenium concentrations and GSH-PX activities than did tissues from virgin mice, but the levels were similar to levels found in preneoplastic and neoplastic mammary tissues of lines C4 and D2. This suggests that the appropriate comparisons for studies determining the effect of selenium on preneoplastic mammary tissues are glands from pregnant and lactating mice. In addition, these results suggest that the refractory state of mammary tumors to selenium-mediated growth inhibition is not due to the absence of GSH-PX or the inability to incorporate selenium. (b) For the second experiment, the effect of feeding various levels of selenium on selenium and GSH-PX levels was determined in mammary and hepatic tissues of virgin mice. GSH-PX activity increased when dietary selenium increased from less than 0.02 to 0.1 ppm selenium but was not further increased when dietary selenium was above 0.1 ppm. (c) Finally, the mammary GSH-PX activity was evaluated at different concentrations of the substrates in order to document the biochemical characteristics of the mammary gland GSH-PX.

Aging↗

PubMed1993

[Influence of selenium-enriched malt on the elevated cGMP concentrations induced by carcinogen].

Rats were fed with selenium-enriched malt containing 1 ppm selenium. As a parameter, cyclic guanosine-3'5'-monophosphate (cGMP) was measured by RIA in the rats following treatment with AFB1. The results demonstrated that the diet containing high selenium inhibited the elevation of cGMP levels in the liver induced by multiple exposures to AFB1 (250 micrograms/kg, 10 times/2 wks), (P < 0.05). Administration of a large single dose of AFB1 (1 mg/kg i.p.) reduced the liver cGMP contents which might be due to injury to the liver. Selenium-enriched diet could prevent this from happening. In high cancer risk areas: the cGMP level in urine of population with higher selenium concentration were lower than that of population with low selenium concentration. A supplementation of 300 micrograms selenium in the form of selenium-enriched malt cakes daily to the subjects with low selenium concentration in blood for one year, the urinary cGMP excretion was significantly decreased from 0.62 mumol/g to 0.49 mumol/g creatinine (P < 0.05). These findings suggest that diet containing high selenium has a protective effect and may play a potential role in cancer chemoprevention.

Aflatoxin B1↗

PubMedDate not supplied

Serum selenium concentrations in patients with newly diagnosed lymphoid malignancies.

BACKGROUND: Increased mortality from lymphoid malignancies following exposure to environmental selenium has recently been reported. Moreover, conflicting results have been found in investigations examining the relationship between serum concentrations of selenium and some clinical features of malignant lymphoproliferative diseases. METHODS: Serum concentrations of selenium were analyzed by atomic absorption spectrometry in fifty-nine patients with newly diagnosed chronic lymphoid malignancies and in forty control subjects. RESULTS: Selenium concentrations were significantly lower in patients than in control subjects. However, when only patients with localized disease were compared to controls, no significant difference in serum selenium concentrations was observed. Clinical stage was inversely associated with selenium levels. High-grade non-Hodgkin's lymphoma was characterized by lower selenium levels than low-grade and intermediate-grade disease. Selenium levels were positively associated with albumin and hemoglobin, and inversely correlated with serum concentrations of beta 2-microglobulin and with erythrocyte sedimentation rate. CONCLUSIONS: The findings of this study do not suggest that a high selenium intake represents a risk factor for malignant lymphoproliferative diseases, but limitations of the investigation hamper evaluation of the results. The possible utility of determining serum concentrations of selenium in the clinical evaluation of patients with lymphoid malignancies merits examination in larger studies.

Double-Blind Method↗

PubMed1996

Serum alpha-tocopherol, vitamin A, and blood selenium concentrations, and glutathione peroxidase activity in llamas fed alfalfa hay.

OBJECTIVES: To measure blood selenium concentration and glutathione peroxidase (GSH-Px) activity and serum concentrations of vitamin A and alpha-tocopherol, and to determine the correlation between blood selenium concentration and GSH-Px activity of llamas fed alfalfa hay. DESIGN: Mean (+/- SD) serum vitamin A and alpha-tocopherol concentrations, blood selenium concentrations, and GSH-Px activity were calculated from 9 sequential blood samples collected from llamas fed a diet of alfalfa hay. ANIMALS: 15 clinically normal llamas (8 males, 7 females) between 10 and 14 months of age. PROCEDURE: Llamas were fed alfalfa hay for 40 days prior to sample collection and then for the duration of the trial. Vitamin E, selenium, and concentrations of vitamin A precursors were measured in the hay. Blood samples were collected on days 0, 6, 7, 9, 13, 20, 42, 64, and 98. Blood selenium concentrations were measured, using an inductively coupled spectrometric method. Blood GSH-Px activity was measured with a spectrophotometer, using a modification of a previously described assay. Isocratic high-performance liquid chromatography with florescent detection was used to determine serum alpha-tocopherol and vitamin A concentrations. RESULTS: The alfalfa hay contained 0.2 mg/kg of selenium, 5 mg/kg of vitamin E, and 0.9 mg/kg of vitamin A precursors. The mean (+/- SD) blood selenium concentration and GSH-Px activity were 0.179 +/- 0.032 micrograms/ml and 25.76 +/- 6.53 mU NADPH oxidized/min/mg of Hb, respectively, with a correlation coefficient of 0.97. The mean (+/- SD) concentrations for serum alpha-tocopherol and vitamin A were 128.1 +/- 41.7 and 74.8 +/- 5.5 micrograms/dl, respectively. CONCLUSIONS: Blood selenium concentrations in llamas are highly correlated to GSH-Px activity. Blood selenium concentrations in llamas appear to be similar to other domestic ruminants and diets containing 0.2 mg/kg of selenium appear to provide an adequate dietary source. The concentrations of vitamin A precursors and vitamin E in the hay were below currently recommended dietary levels for llamas, and alfalfa hay appears to provide an unreliable source of vitamins A and E in this species. Further studies are required to determine optimal dietary concentrations and to substantiate a reference range for these vitamins in llamas.

Animal Feed↗

PubMedDate not supplied

Modulation by selenium supplementation of lipid peroxidation induced by chronic administration of adriamycin in rats.

Adriamycin (doxorubicin) is an antineoplastic drug used to treat various cancers; however, its chronic use is accompanied by cardiotoxicity. Previous results suggested that free radical formation may contribute to Adriamycin toxicity. Adriamycin-induced cardiotoxicity was examined in rats maintained on either standard or selenium-supplemented diets. Adriamycin was administered intraperitoneally; the cumulative dose was 15 mg/kg body weight. Selenium status, glutathione peroxidase activities, vitamin E, and MDA contents were determined on red blood cell (RBC) and cardiac homogenates. RBC selenium levels and selenium glutathione peroxidase activity were significantly increased in selenium-supplemented animals compared with control or placebo groups. However, Adriamycin-treated rats showed a significant decrease in RBC selenium and selenium glutathione peroxidase compared with the placebo group. Moreover, treatment with Adriamycin increased RBC MDA content, which was attenuated by the selenium supplementation. In parallel, RBC vitamin E decreased markedly in the Adriamycin-treated group and was totally restored by selenium supplementation. Cardiac biochemical analyses confirmed the blood results. Thus, a free radical mechanism does contribute to Adriamycin cardiotoxicity, and shows the importance of balancing selenium levels in Adriamycin-treated subjects to limit Adriamycin's action. A decrease in Adriamycin cardiotoxicity with no concomitant decrease in its antineoplastic activity would considerably improve the therapeutic benefit of the drug.

Animals↗

PubMed1996

[Selenium status of healthy children under 1 year of age dependent on the type of feeding].

Selenium status was studied in 70 healthy children under 1 year of age being on breastfeeding or bottle feeding. Selenium status was determined by analysis of selenium in baby's hairs and nails. Selenium was also analyzed in breast milk in course of the lactation and in breast milk substitutes. The selenium status was better in breastfed children than in bottle fed ones. The most high level of selenium was found in breast milk in first month of lactation. Selenium status of bottle fed children was depended on selenium level in milk substitutes. It is necessary further investigations on selenium status of children under 1 year age to elaborate and suggest the standard level of selenium contents in milk substitutes.

Age Factors↗

PubMed1997

Observations on the efficacy of various forms of selenium for livestock: a review.

Since 1957, selenium has found extensive use in livestock production to maintain an adequate selenium status in animals in areas of soil and feed/forage deficiency. Selenium may be given directly to livestock, or applied as a fertilizer amendment to increase selenium content of their feeds. This paper addresses the area of direct supplementation, which includes oral and parenteral supplementation, and with ruminant animals the use of slow-release boluses. Various chemical forms of selenium have been examined as supplemental sources, with sodium selenite being the earliest compound of choice. Combination of selenium supplementation with other livestock management practices led to use of selenium dioxide, which avoided solubility problems with selenite but produced effective responses. Barium salts have been used with some success as supplemental selenium sources. Experience with ruminal boluses has shown that high pressure pelleting of increased grain size selenium, in hollow pellets, has prolonged their useful life. Attention has been paid recently to residual selenium returned to the soil from livestock supplementation practices and the resulting opinion is that currently approved practices are acceptable from the point of view of environmental quality.

Animal Feed↗

PubMed1998

[Effect of dietary selenium on the activity of UDP-glucuronosyltransferases and metabolism of mycotoxin deoxynivalenol in rats].

The influence of selenium excess and deficiency on the activity of xenobiotic metabolizing enzymes and the metabolism of mycotoxin deoxynivalenol (DON) in rats was studied. Wistar male rats were fed for 6 weeks semi-synthetic diets containing 0.2, 1.0 or 5.0 ppm selenium. For induction of selenium deficiency the weanling rats were fed for 6 weeks diet containing < or = 0.02 ppm selenium. The activity of selenium-dependent glutathione peroxidase was reduced in the liver of selenium-deficient rats by 93% at 42 days. DON, its de-epoxy metabolite DOM-1, DON and DOM-1 glucuronides were analyzed by reverse-phase HPLC in urine and feces after the single oral dose of DON (8 mg/kg). Selenium-supplemented (5 ppm) diet increased by 2-3 times formation and elimination of DON and DOM-1 glucuronides in urine. Selenium-deficient diet decreased formation of DOM-1, but increased significantly total excretion of DON and DON glucuronides. The activity of GT1 and GT2 forms of UDP-glucuronosyltransferase, an enzyme principally responsible for glucuronidation, was two times higher in the liver of rats fed both selenium-supplemented and selenium-deficient diets.

Administration, Oral↗

PubMed1998

[Selenium status and bronchopulmonary dysplasia in premature infants <1,500 g].

Selenium is an essential component of the antioxidant enzyme glutathione peroxidase that protects tissues against oxidative injury by detoxifying peroxides. In preterm infants the risk for selenium deficiency is increased due to insufficient selenium uptake. Low selenium uptake and as a consequence decreased glutathione peroxidase activity may result in an elevated risk for the development of bronchopulmonary dysplasia (BPD). The aim of this prospective study was to investigate the relationship between the selenium status of preterm infants < 1500 g and the incidence of BPD. We determined the selenium plasma levels by means of atomic absorption spectrometry in 34 VLBW infants (mean birth weight 1075 +/- 249 g; mean gestational age 28.6 +/- 2.5 weeks) within the first 5 days of life and later in the age of 4 weeks. The infants received mainly parenteral nutrition and were not specifically supplied with selenium. Postnatally, the selenium plasma level was 34.2 micrograms/l (17.3/50) [median (25/75% quantil)] and dropped after 4 weeks to a median value of 16.1 micrograms/l (5.2/38.4) (p < 0.001). In the infants with BPD (n = 12) the selenium concentration within the first week of life was 45.0 micrograms/l (31.5/55.6) versus 33.2 micrograms/l (20.2/42.4) in the infants without BPD. In the age of 4 weeks of life the median selenium level was not significantly different between the infants with and without BPD - 17.2 micrograms/l (10.3/22.5) versus 14.8 micrograms/l (8.8/22.6).

Bronchopulmonary Dysplasia↗

PubMed1997

[Effect of selenium administration on various laboratory parameters of patients at risk for sepsis syndrome].

BACKGROUND: Low selenium plasma levels were often measured in ICU patients with polytrauma, major surgery or various severe diseases. Activation of selenium-dependent functions of the antioxidant metabolism and the immune system is suggested to be causally. METHODS: In a prospective randomized clinical trial including 24 critically ill patients we investigated the plasma levels of selenium, malondialdehyde, glutathione, elastase, fT3, fT4, TSH, IL-2R, IL-6 and IL-8 with and without parenteral selenium supplementation for 3 weeks (study design: week 1: twice 500 micrograms daily, week 2: once 500 micrograms, week 3: three times 100 micrograms sodium selenite). RESULTS: Following 24 hours of supplementation selenium plasma levels were normalized. Malondialdehyde level decreased in the therapy group significantly beginning at day 3. In the control group we observed increased malondialdehyde values, a disturbed glutathione metabolism and an elevated elastase activity. fT3-values were diminished at day 0 in all patients. In the therapy group we measured a gradual fT3 restoration. In the control group a reactive TSH increase was observed. Selenium supplementation did not lead to an excessive stimulation of IL-2R, IL-6 or IL-8. CONCLUSIONS: 1. Rapid normalization of selenium plasma levels can be achieved with the applied selenium dosage. 2. Parameters of radical metabolism are significantly reduced following selenium administration. 3. T3 synthesis correlates closely with the selenium levels. 4. Excessive stimulation of the immune system does not appear in the applied dosage.

Adult↗

PubMed2000

Selenate-supplemented nutritional formula increases plasma selenium in hemodialysis patients.

OBJECTIVE: The purpose of this study was to determine the short-term effect of feeding selenium-supplemented formulas on the selenium status of end-stage renal disease patients on hemodialysis. DESIGN AND SETTING: The prospective, randomized, single-blind study of parallel design was conducted at three hemodialysis clinics. PATIENTS: A total of 79 hemodialysis patients were randomly assigned into one of three groups. INTERVENTION: Liquid nutritional formula supplemented with either selenite (28 microg Se/8 oz, n = 26), selenate (28 microg Se/8 oz, n = 26), or nonfortified (7 microg Se/8 oz, n = 27) was fed to hemodialysis patients as their sole source of nutrition for 14 days. MAIN OUTCOME MEASURE: Plasma and red blood cell (RBC) selenium and glutathione peroxidase (GPX) activities were measured in predialysis blood both before (day 1) and after (day 8) a 7-day baseline period, and after subjects received the formula as the sole source of nutrition (approximately 35 kcal/kg/d) for 14 days (day 22). RESULTS: Selenium intake (Mean +/- SEM, microg/d) was 134 +/- 9, 140 +/- 9, and 35 +/- 2 for patients receiving selenite-, selenate-, or non-supplemented formula, respectively. On day 22, plasma selenium (micromol/L) was greater (P <.032) in the selenate-supplemented group (1.5 +/- 0.1) compared with the nonsupplemented group (1.2 +/- 0.1), but not compared with the selenite-supplemented group (1.4 +/- 0.1). Plasma GPX activity was 44% to 60% that of healthy controls and not different among groups. RBC selenium and GPX activities were within the normal range and were not different among groups. CONCLUSION: The results of this study indicate that a liquid formula supplemented with selenium as selenate is successful at maintaining selenium concentrations within normal range, as well as significantly increasing plasma selenium levels compared with nonsupplementation.

Adult↗

PubMed1999

Selenium redox biochemistry of zinc-sulfur coordination sites in proteins and enzymes.

Selenium has been increasingly recognized as an essential element in biology and medicine. Its biochemistry resembles that of sulfur, yet differs from it by virtue of both redox potentials and stabilities of its oxidation states. Selenium can substitute for the more ubiquitous sulfur of cysteine and as such plays an important role in more than a dozen selenoproteins. We have chosen to examine zinc-sulfur centers as possible targets of selenium redox biochemistry. Selenium compounds release zinc from zinc/thiolate-coordination environments, thereby affecting the cellular thiol redox state and the distribution of zinc and likely of other metal ions. Aromatic selenium compounds are excellent spectroscopic probes of the otherwise relatively unstable functional selenium groups. Zinc-coordinated thiolates, e.g., metallothionein (MT), and uncoordinated thiolates, e.g., glutathione, react with benzeneseleninic acid (oxidation state +2), benzeneselenenyl chloride (oxidation state 0) and selenocystamine (oxidation state -1). Benzeneseleninic acid and benzeneselenenyl chloride react very rapidly with MT and titrate substoichiometrically and with a 1:1 stoichiometry, respectively. Selenium compounds also catalyze the release of zinc from MT in peroxidation and thiol/disulfide-interchange reactions. The selenoenzyme glutathione peroxidase catalytically oxidizes MT and releases zinc in the presence of t-butyl hydroperoxide, suggesting that this type of redox chemistry may be employed in biology for the control of metal metabolism. Moreover, selenium compounds are likely targets for zinc/thiolate coordination centers in vivo, because the reactions are only partially suppressed by excess glutathione. This specificity and the potential to undergo catalytic reactions at low concentrations suggests that zinc release is a significant aspect of the therapeutic antioxidant actions of selenium compounds in antiinflammatory and anticarcinogenic agents.

Animals↗

PubMed1991

Levels and 75Se-labeling of specific proteins as a consequence of dietary selenium concentration in mice and rats.

Selenium-labeled proteins (SLP) distinct from glutathione peroxidase (GSH-PX) recently have been purified and partially characterized. Antisera to two SLP, a 56-kDa and a 14-kDa protein, were generated in rabbits and used to examine expression of these proteins as a consequence of dietary selenium concentration (0.02, 0.2, 2.0 ppm) in mice and rats. Additionally, the kinetics of 75Se labeling in plasma, liver, kidney, and mammary gland were examined over a 40-hr time period as a function of dietary selenium concentration. A plasma 57-kDa protein was labeled by 30 min after 75Se injection and reached maximum labeling by 4 hr. The cellular 56-kDa and 14-kDa proteins, as well as GSH-Px, labeled progressively over 40 hr starting between 1 and 4 hr after injection. In general, the 56-kDa and GSH-Px followed similar labeling patterns, whereas the 14-kDa protein was labeled less and was not labeled in discernible quantities until 40 hr. The extent of labeling of all proteins was inversely proportional to the dietary selenium concentration and was probably a reflection of different endogenous selenium body pools. The most important observation was generated by the immunoblot data. The amount of 56-kDa and 14-kDa proteins as detected and measured on immunoblots was not a function of dietary selenium concentration. This result suggests that the synthesis and maintenance of the 56-kDa and 14-kDa proteins are not selenium dependent, a characteristic which distinguishes the two proteins from GSH-Px. The single exception to the above results was the 40% decrease of liver 14-kDa protein concentration in carcinogen-treated rats fed 2.0 ppm of selenium. An organic selenium compound, selenobetaine, did not lead to a decrease under similar conditions. In 15 rat mammary tumors induced by 7,12-dimethylbenzanthracene and analyzed on immunoblots, the SLP-56 was undetected in 5 cases and appeared as two bands (56,000 Da, 50,000 Da) in 10 cases. This latter result raises the possibility that the expression of SLP-56 may be altered in mammary tumors as compared with normal mammary gland.

Animals↗

PubMed1989

Toxicosis in pigs fed selenium-accumulating Astragalus plant species or sodium selenate.

Three groups of 5 pigs each were fed a high selenium (Se) diet by mixing either Astragalus praelongus (31.6 ppm Se in feed), A bisulcatus (31.7 ppm Se in feed), or sodium selenate (26.6 ppm Se in feed) with commercial hog feed. Ten control pigs were fed only commercial hog chow containing trace selenium (0.44 ppm Se). Pigs were fed for 9 weeks and necropsied when they had ataxia or paralysis. Blood was collected for hematologic and serum biochemical determinations, and samples of various tissues were collected and fixed in neutral-buffered 10% formalin for histologic evaluation or frozen for determination of selenium concentration. All forms of selenium induced clinical signs of weight and hair loss, with cracked hooves and inflamed coronary bands developing in all Na2SeO4-fed pigs and 1 A praelongus-fed pig, but not in A bisulcatus-fed pigs. Serum calcium, phosphorus, and albumin concentrations were unchanged or significantly decreased from prefeeding values in groups fed selenium. Serum aspartate transaminase (AST) activities in Astragalus species-fed groups, and amylase activities and PCV in all groups of pigs fed selenium, were increased. Serum alkaline phosphatase and creatine kinase activities were significantly increased in the A praelongus-fed pigs and significantly decreased in Na2SeO4-fed pigs. Terminal tissue and body fluid selenium concentrations were determined in all groups of pigs fed selenium and compared with values in control pigs. Urine and bile concentrations were increased by the greatest factor (40 to 100x), with tissue concentrations of selenium increased by a lesser factor (6 to 17x).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1984

Selenium inhibition of DNA synthesis in mouse mammary epithelial cell line YN-4.

Previous results have documented that Na2SeO3 has a biphasic effect on the growth of mammary cells in vitro. In the experiments reported herein, the effects of selenium on several parameters of cell proliferation in the YN-4 mouse mammary cell line were investigated. The biphasic effect of selenium on cell growth was confirmed; i.e., 5 X 10(-8) M selenium stimulated cell growth, whereas 5 X 10(-6) M delayed cell growth and 5 X 10(-5) M was cytotoxic. The inhibition of cell growth by 5 X 10(-6) M selenium was reversible when this dose was removed from the growth medium. The increased cell growth at 5 X 10(-8) M selenium was reflected by an increased cell number, increased uptake of [3H]thymidine into DNA, increased DNA labeling index, and an increased rate of DNA synthesis. The decreased cell growth at 5 X 10(-6) M selenium was reflected by a decrease in all of these parameters of cell growth kinetics. The differential effects of selenium were manifested by 48 hr after addition of selenium to the cell culture medium. The results indicate that one of the mechanisms of selenium-mediated inhibition of carcinogenesis may be due to an inhibition of cell proliferation of responsive cells.

Animals↗

PubMed1995

Comparison of 1% and 2.5% selenium sulfide in the treatment of tinea capitis.

OBJECTIVE: To determine whether an over-the-counter shampoo containing 1% selenium sulfide would have sporicidal activity equal to that of a 2.5% selenium sulfide prescription lotion in the adjunctive treatment of tinea capitis infection. DESIGN: Prospective randomized nonblinded clinical trial. SETTING: Outpatient clinics and emergency department of a children's hospital. PATIENTS: Fifty-four patients between the ages of 1 and 15 years with culture-proved tinea capitis infection caused by Trichophyton tonsurans enrolled during a 14-month period. METHODS: Patients were randomized to receive 2.5% selenium sulfide lotion, 1% selenium sulfide shampoo, or a bland, nonmedicated shampoo with which they were instructed to shampoo twice weekly. All received 15 mg/kg per day of griseofulvin. Dermatophyte cultures of the affected area of each patient's scalp were obtained on enrollment and every 2 weeks until a negative culture was obtained from a previously infected area. RESULTS: Survival data analysis demonstrated that both the 2.5% selenium sulfide and 1% selenium sulfide preparations were superior to the nonmedicated control shampoo in terms of the time required to eliminate shedding of viable spores. When compared with each other, there was no difference between the 2.5% selenium sulfide and 1% selenium sulfide preparations in time required to produce a negative culture. CONCLUSION: Commercially available 1% selenium sulfide shampoo is an equally effective yet less expensive alternative sporicidal therapy in the adjunctive treatment of tinea capitis infection.

Adolescent↗